Pathophysiology of white-nose syndrome in bats: a mechanistic model linking wing damage to mortality.

White-nose syndrome is devastating North American bat populations but we lack basic information on disease mechanisms. Altered blood physiology owing to epidermal invasion by the fungal pathogen Geomyces destructans (Gd) has been hypothesized as a cause of disrupted torpor patterns of affected hibernating bats, leading to mortality. Here, we present data on blood electrolyte concentration, haematology and acid-base balance of hibernating little brown bats, Myotis lucifugus, following experimental inoculation with Gd. Compared with controls, infected bats showed electrolyte depletion (i.e. lower plasma sodium), changes in haematology (i.e. increased haematocrit and decreased glucose) and disrupted acid-base balance (i.e. lower CO2 partial pressure and bicarbonate). These findings indicate hypotonic dehydration, hypovolaemia and metabolic acidosis. We propose a mechanistic model linking tissue damage to altered homeostasis and morbidity/mortality.

Univariate and multivariate analysis of risk factors for severe Clostridium difficile-associated diarrhoea: importance of co-morbidity and serum C-reactive protein.

AIM: To investigate risk factors for severe clostridium difficile associated diarrhoea (CDAD) in hospitalised patients. METHODS: We analysed risk factors for severe CDAD (associated with systemic signs of hypovolemia) in 124 hospitalised patients by retrospective chart review. RESULTS: Severe CDAD was present in 27 patients (22%). Statistical analysis showed a significant association with a higher 30-d mortality (33% vs 4%, P < 0.001) and a higher proportion of longer hospital stay exceeding 14 d (74% vs 52%, P = 0.048). Charlson co-morbidity score (OR 1.29 for 1 point increment, P < 0.05) and serum C-reactive protein at diagnosis (OR 1.15 for 10 mg/L increment, P < 0.001) were independent predictors of severe CDAD. CONCLUSION: Patients with a severe level of co-morbidity and high serum C-reactive protein levels at the time of diagnosis should receive particular attention.

[Volume expansion during septic shock]. / Le remplissage vasculaire au cours du choc septique.

At its very early phase, septic shock is characterized by severe hypovolemia related to abundant fluid losses, increased venous compliance and maldistribution of extracellular fluid (interstitial edema, splanchnic pooling). It results in a drop in venous return and cardiac output. Volume expansion, with crystalloids or colloids produces a hyperdynamic state with high cardiac output and low peripheral resistances. The quantity of liquid administered rather than its composition is the main determinant. Clinical examination and hemodynamic monitoring (Swan-Ganz catheter) appear to provide the most useful criteria to assess the limits of liquid administration. Better understanding in the mechanisms of circulatory dysfunction due to the inflammation cascades might soon lead to a new approach in fluid therapy.